A Review of Time Courses and Predictors of Lipid Changes with Fenofibric Acid-Statin Combination

Fibrates activate peroxisome proliferator activated receptor α and exert beneficial effects on triglycerides, high-density lipoprotein cholesterol, and low density lipoprotein subspecies. Fenofibric acid (FA) has been studied in a large number of patients with mixed dyslipidemia, combined with a low- or moderate-dose statin. The combination of FA with simvastatin, atorvastatin and rosuvastatin resulted in greater improvement of the overall lipid profile compared with the corresponding statin dose. The long-term efficacy of FA combined with low- or moderate- dose statin has been demonstrated in a wide range of patients, including patients with type 2 diabetes mellitus, metabolic syndrome, or elderly subjects. The FA and statin combination seems to be a reasonable option to further reduce cardiovascular risk in high-risk populations, although trials examining cardiovascular disease events are missing

Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease

Antonia Pagkali,1 Anastasios Makris,1 Kalliopi Brofidi,2 Aris P Agouridis,3,4 Theodosios D Filippatos2 1School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 2Department of Internal Medicine, School of Medicine, University of Crete, Heraklion, Greece; 3School of Medicine, European University Cyprus, Nicosia, Cyprus; 4Department of Internal Medicine, German Oncology Center, Limassol, CyprusCorrespondence: Theodosios D Filippatos, Department of Internal Medicine, School of Medicine, University of Crete, Heraklion, Greece, Tel + (30)2810392960, Fax + (30)2810392359, Email [email protected]: Non-Alcoholic Fatty Pancreas disease (NAFPD), characterized by fat accumulation in pancreatic tissue, is an emerging clinical entity. However, the clinical associations, the underlying molecular drivers, and the pathophysiological mechanisms of NAFPD have not yet been characterized in detail. The NAFPD spectrum not only includes infiltration and accumulation of fat within and between pancreatic cells but also involves several inflammatory processes, dysregulation of physiological metabolic pathways, and hormonal defects. A deeper understanding of the underlying molecular mechanisms is key to correlate NAFPD with clinical entities including non-alcoholic fatty liver disease, metabolic syndrome, diabetes mellitus, atherosclerosis, as well as pancreatic cancer and pancreatitis. The aim of this review is to examine the pathophysiological mechanisms of NAFPD and to assess the possible causative/predictive risk factors of NAFPD-related clinical syndromes.Keywords: non-alcoholic fatty pancreas disease, NAFPD, steatotic pancreatic disease, metabolic dysfunction-associated steatotic pancreatic disease, MASP